A major cause of heart disease and stroke is the formation and persistence of aberrant clots that block the flow of blood. The predominant clot busting medicine is tissue plasminogen activator (tPA) and its recombinant derivatives. The main medical and commercial problems with tPA are that: 1) it may cause hemorrhage most likely because it is a functional enzyme exhibiting detrimental systemic effects; 2) about half of patients' clots are resistant to tPA and 3) it has only ˜4% penetrance into the target market because of a finite time of efficacy (3-5 hours after the onset of symptoms).
It would be highly desirable to be provided with a safer therapeutic agent capable of accelerating the dissolution of a clot and/or preventing the formation of a clot. When used alone, the safer therapeutic agent would preferably have limited or no undesirable systemic effect (such as bleeding for example). When used in combination with known clot-busting medicine, the safer therapeutic agent would preferably increase the thrombolytic potential of the combined known clot-busting medicine, reduce the dose required of the known clot-busting medicine to observe beneficial therapeutic effects and ultimately limit the side effects associated with known clot-busting medicine.